Fluorescein angiography (FA) is generally accepted among the nephrology community as being kidney friendly; however, it remains unclear whether it is truly safe or not based on the available evidence. were There have been three retrospective studies [1],[2],[3] and two prospective ones [4],[5] ([Table 1]) published till now examining the effect of FA on kidney functions. When pooling data from these studies, 16 patients (of 618, 2.5%) developed acute kidney injury (AKI) [defined as an absolute increase in serum creatinine (SCr) ≥0.5 mg/dl or ≥25% increase from baseline within 24–72 h after FA]. Most of the studies reported that SCr level returned back to normal within few days without any intervention, or attributed the increase in SCr level to an associated event (e.g. concomitant nephrotoxic drug administration).

Nevertheless, these studies had many limitations, including first, the absence of long-term follow-up data. It has to be noted that the peak rise in SCr level may occur 5 days or even more after contrast exposure [6]. The second was the use of 0.5 mg/dl absolute increase in SCr as a cutoff point to define contrast induced nephropathy (CIN) rather than the 0.3 mg/dl absolute rise recommended by AKIN [7] and KDIGO [8] guidelines. Even though decreasing the threshold from 0.5 to 0.3 mg/dl may falsely identify patients with AKI owing to assay variability and day-to-day variability, early detection is more important. Third, the use of SCr and estimated glomerular filtration rate as a marker for CIN development, despite being the current accepted definition, it still got some limitations. SCr has been inferior to serum cystatin-C, urinary (or serum) neutrophil gelatinase-associated lipocalin, urinary KIM-1, and interleukin-18 in early detection of CIN [9],[10],[11],[12]. Testing these early AKI biomarkers (namely serum cystatin-C and urinary neutrophil gelatinase-associated lipocalin) after FA detected more cases with CIN rather than SCr ([Table 1]) [4].

Despite these limitation, and in the view of the current evidence and clinical practice, one cannot prohibit FA for patients at risk of CIN, especially patients with chronic kidney disease as long as it is clinically indicated. However, patients and clinicians should be aware of the absence of long-term safety data, the potential hazard of subclinical AKI and the need for further clinical trials to assess and assure the long-term safety of FA.